Motolimod (VTX-2337) analog and a toll-like receptor 8 (TLR8)-selective agonist with stronger activity than resiquimod (R848) and CL075 (3M002).
TL8-506 is a motolimod (VTX-2337) analog and a benzoazepine class toll-like receptor 8 (TLR8)-selective agonist. TL8-506 is commonly employed in the concentration range from 0.1 μg/mL to 1 μg/mL for stimulating cell surface TLR8 in cultures and is reported to be a stronger TLR8 ligand than the imidazoquinoline (IMDQ) derivatives (IQDs) resiquimod (R848) and CL075 (3M002).
Human trichinellosis is acquired by eating raw or undercooked meats carrying muscle larvae of Trichinella spp. Toll-like receptors (TLRs) are essential components of the innate immune system. However, little is known about the potential application of TLR agonists for immunotherapy
Messenger RNA (mRNA) represents an attractive therapeutic modality for potentially a wide range of clinical indications but requires uridine chemistry modification and/or tuning of the production process to prevent activation of cellular innate immune sensors and a concomitant reduction in
Human Vγ9Vδ2 γδ T cells can kill a variety of cancer cells and have attracted substantial interest for cancer immunotherapy. Toll-like receptor (TLR) ligands are promising adjuvants for cancer immunotherapy, but TLR7/8 ligand Resiquimod has been shown to inhibit CD4
Human toll-like receptor 8 (TLR8) activation induces a potent T helper-1 (Th1) cell response critical for defense against intracellular pathogens, including protozoa. The receptor harbors two distinct binding sites, uridine and di- and/or trinucleotides, but the RNases upstream of TLR8
Inborn errors of immunity (IEI) are a genetically heterogeneous group of disorders with a broad clinical spectrum. Identification of molecular and functional bases of these disorders is important for diagnosis, treatment, and an understanding of the human immune response. We
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